Low back pain is a leading cause of disability and lost productivity. Up to 90% of adults experience back pain at some time during their lives. For frequency of physician visits, back pain is second only to upper respiratory infections. In the United States the economic impact of this malady has been reported to range from $50-$100 billion each year, disabling 5.2 million people. Though the sources of low back pain are varied, in many cases the intervertebral disc is thought to play a central role. Degeneration of the disc initiates pain in other tissues by altering spinal mechanics and producing non-physiologic stress in surrounding tissues.
The intervertebral disc 100 absorbs most of the compressive load of the spine, but the facet joints 142, 143 of the vertebral bodies 159 share approximately 16%. The disc 100 consists of three distinct parts: the nucleus pulposus 128, the annular layers and the cartilaginous endplates 105, as shown in FIGS. 1 and 2. The disc 100 maintains its structural properties largely through its ability to attract and retain water. A normal disc 100 contains 80% water in the nucleus pulposus 128. The nucleus pulposus 128 within a normal disc 100 is rich in water absorbing sulfated glycosaminoglycans, creating the swelling pressure to provide tensile stress within the collagen fibers of the annulus. The swelling pressure produced by high water content is crucial to supporting the annular layers for sustaining compressive loads, as shown in a longitudinal view in FIG. 2.
In adults, the intervertebral disc 100 is avascular. Survival of the disc cells depends on diffusion of nutrients from external blood vessels 112 and capillaries 107 through the cartilage 106 of the endplates 105, as shown in FIG. 2. Diffusion of nutrients also permeates from peripheral blood vessels adjacent to the outer annulus, but these nutrients can only permeate up to 1 cm into the annular layers of the disc 100. An adult disc can be as large as 5 cm in diameter; hence diffusion through the cranial and caudal endplates 105 is crucial for maintaining the health of the nucleus pulposus 128 and inner annular layers of the disc 100.
Calcium pyrophosphate and hydroxyapatite are commonly found in the endplate 105 and nucleus pulpous 128. As young as 18 years of age, calcified layers 108 begin to accumulate in the cartilaginous endplate 105, as shown in FIG. 3. The blood vessels 112 and capillaries 107 at the bone-cartilage interface are gradually occluded by the build-up of the calcified layers 108, which form into bone. Bone formation at the endplate 105 increases with age.
When the endplate 105 is obliterated by bone, diffusion between the nucleus pulposus 128 and blood vessels 112 beyond the endplate 105 is greatly limited. In addition to hindering the diffusion of nutrients, calcified endplates 105 further limit the permeation of oxygen into the disc 100. Oxygen concentration at the central part of the nucleus 128 is extremely low. Cellularity of the disc 100 is already low compared to most tissues. To obtain necessary nutrients and oxygen, cell activity is restricted to being on or in very close proximity to the cartilaginous endplate 105. Furthermore, oxygen concentrations are very sensitive to changes in cell density or consumption rate per cell.
The supply of sulfate into the nucleus pulposus 128 for biosynthesizing sulfated glycosaminoglycans is also restricted by the calcified endplates 105. As a result, the sulfated glycosaminoglycan concentration decreases, leading to lower water content and swelling pressure within the nucleus pulposus 128. During normal daily compressive loading on the spine, the reduced pressure within the nucleus pulposus 128 can no longer distribute the forces evenly along the circumference of the inner annulus to keep the lamellae bulging outward. As a result, the inner lamellae sag inward, while the outer annulus continues to bulge outward, causing delamination 114 of the annular layers, as shown in FIGS. 3 and 4.
The shear stresses causing annular delamination and bulging are highest at the posteriolateral portions adjacent to the neuroforamen 121. The nerve 194 is confined within the neuroforamen 142 between the disc and the facet joint 142, 143. Hence, the nerve 194 at the neuroforamen 121 is vulnerable to impingement by the bulging disc 100 or bone spurs.
When oxygen concentration in the disc falls below 0.25 kPa (1.9 mm Hg), production of lactic acid dramatically increases with increasing distance from the endplate 105. The pH within the disc 100 falls as lactic acid concentration increases. Lactic acid diffuses through micro-tears of annulus irritating the richly innervated posterior longitudinal ligament 195, facet joint and/or nerve root 194. Studies indicate that lumbar pain correlates well with high lactate levels and low pH. The mean pH of symptomatic discs was significantly lower than the mean pH of the normal discs. The acid concentration is three times higher in symptomatic discs than normal discs. In symptomatic discs with pH 6.65, the acid concentration within the disc is 5.6 times the plasma level. In some preoperative symptomatic discs, nerve roots 194 were found to be surrounded by dense fibrous scars and adhesions with remarkably low pH 5.7-6.30. The acid concentration within the disc was 50 times the plasma level.
Approximately 85% of patients with low back pain cannot be given a precise pathoanatomical diagnosis. This type of pain is generally classified under “non-specific pain”. Back pain and sciatica can be recapitulated by maneuvers that do not affect the nerve root, such as intradiscal saline injection, discography, and compression of the posterior longitudinal ligaments. It is possible that some of the non-specific pain is caused by lactic acid irritation secreted from the disc. Injection into the disc can flush out the lactic acid. Maneuvering and compression can also drive out the irritating acid to produce non-specific pain. Currently, no intervention other than discectomy can halt the production of lactic acid.
The nucleus pulposus 128 is thought to function as “the air in a tire” to pressurize the disc 100. To support the load, the pressure effectively distributes the forces evenly along the circumference of the inner annulus and keeps the lamellae bulging outward. The process of disc degeneration begins with calcification of the endplates 105, which hinders diffusion of sulfate and oxygen into the nucleus pulposus 128. As a result, production of the water absorbing sulfated glycosaminoglycans is significantly reduced, and the water content within the nucleus decreases. The inner annular lamellae begin to sag inward, and the tension on collagen fibers within the annulus is lost. The degenerated disc 100 exhibits unstable movement, similar to a flat tire. Approximately 20-30% of low-back-pain patients have been diagnosed as having spinal segmental instability. The pain may originate from stress and increased load on the facet joints and/or surrounding ligaments. In addition, pH within the disc 100 becomes acidic from the anaerobic production of lactic acid, which irritates adjacent nerves and tissues.
Resilient straightening of a super elastically curved needle within a rigid needle is described in prior art DE 44 40 346 A1 by Andres Melzer filed on Nov. 14, 1994 and FR 2 586 183-A1 by Olivier Troisier filed on Aug. 19, 1985. The curved needles of these prior art are used to deliver liquid into soft tissue. In order to reach the intervertebral disc without an external incision, the lengths of the curved and rigid needles must be at least six inches (15.2 cm). There are multiple problems when attempting to puncture the calcified endplate as described in the prior art. Shape memory material for making the curved needle usually is elastic. Nickel-titanium alloy has Young's modulus approximately 83 GPa (austenite), 28-41 GPa (martensite). Even if the handles of both the curved and rigid needles are restricted from twisting, the long and elastically curved needle 101 is likely to twist within the lengthy rigid needle 220 during endplate 105 puncturing, as shown in FIGS. 54 and 55. As a result, direction of puncture is likely to be deflected and endplate 105 puncture would fail.
Furthermore, in the prior art, the sharp tips of their rigid needles are on the concave sides of the curved needles. When puncturing a relatively hard tissue, such as calcified endplates 105, the convex sides of the curved needles are unsupported and vulnerable to bending, resulting in failure to puncture through the calcified endplates 105. To minimize bending or twisting, the sizes of their curved and rigid needles are required to be large. By increasing the sizes of the curved 101 and rigid 220 needles, friction between the curved 101 and rigid 220 needles greatly increases, making deployment and retrieval of the curved needle 101 very difficult. In addition, a large opening created in the disc 100 by the large needles may cause herniation of the nucleus pulposus 128. Similarly, a large opening at the endplate 105 may cause Schmorl's nodes, leakage of nucleus pulpous 128 into the vertebral body 159.
In essence, the support from the distal end of the rigid needle 220 in FIGS. 62-67 of this invention is relevant to support puncturing of a relatively hard tissue, such as calcified endplate 105 with a small diameter needle 101. Furthermore, the non-round cross-sections of the curved 101 and rigid 220 needles in FIGS. 56-60 to prevent twisting are also relevant to ensure successful puncturing through the calcified endplate 105.